The prevalence of asthma has increased over the 20th century in most, if not all, developed countries of the world. Major findings from the European Community Respiratory Health Survey and the International Study of Asthma and Allergies in Childhood were that asthma prevalence is increasing worldwide;is generally more common in Western countries;more prevalent in English-speaking countries;and increasing in developing countries as they become more Westernized or become urbanized. CDC estimated that from January to March of 2006 more than 22 million Americans (8.0%) suffered from asthma, an increase from 7.8% in 2005. While many studies have demonstrated strong inherited influences on the development of asthma, these changes have been too rapid to be explained solely by genetics, and it has been widely hypothesized that early life exposures influence an infant[unreadable]s susceptibility to asthma. In the US, asthma morbidity and mortality are highest among persons who are of minority status. One approach to reducing racial disparities involves targeting reductions in asthma incidence through modification of risk factors. The objective of this proposal is the epidemiological investigation of early life environmental factors, focusing on pet exposure and endotoxin, that may alter immunologic development, based on the premise that variations in the early immune response to environmental stimuli affects risk for asthma.The level of exposure of humans to animals (and presumably endotoxin) has declined over the last 100 years through urbanization and suburbanization, although humans have evolved with close contact with animals. As part of an ongoing study, the Wayne County Health, Environment, Allergy &Asthma Longitudinal Study (WHEALS), a multi-ethnic cohort of pregnant women has been recruited for prospective study of their children. With this renewal, we will extend follow-up to 5-6 years of age for the 1248 children of varied racial backgrounds (60% Black). We will use the WHEALS cohort to 1) evaluate whether pet contact and household endotoxin levels affect total and allergen-specific IgE and extracellular cytokine (IL4, IL5, IL13, IFN?, IL2, IL12, TNF and IL10 production by stimulated T-cells) patterns measured at 4 points in time during infancy (birth, 6 months, 12 months and 2 years) and 2) how these exposures and immunological patterns are related to the prevalence of clinical asthma at age 5-6 years. Finally, the data will be analyzed to evaluate the role that Black race plays in the relationship between early environmental exposures and immunological biomarkers and asthma, after accounting for other non-modifiable and modifiable risk factors including CD14 genotype, family history, child sex, birth order, birth characteristics, socioeconomic status, and other social, behavioral and environmental variables. If factors associated with animal or endotoxin contact are related to asthma risk, such factors would likely lend themselves to public health interventions.